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目的:探索哺乳动物雷帕霉素靶蛋白mTORC1和mTORC2在前列腺癌22RV1细胞增殖及凋亡中的作用。方法:噻唑蓝(MTT)比色法检测mTORC1和mTORC2沉默后前列腺癌22RV1细胞增殖改变;流式细胞术(FCM)检测mTORC1和mTORC2沉默后前列腺癌22RV1细胞凋亡;Western印迹检测mTORC1和mTORC2沉默后前列腺癌22RV1细胞雄激素受体(AR)和Akt磷酸化表达。结果:MTT显示mTORC1沉默后,前列腺癌22RV1细胞的生长率无明显变化(P>0.05),而mTORC2沉默后,细胞的增殖受到了显著抑制(P<0.01);FCM显示mTORC1沉默后,细胞的凋亡率明显增加(P<0.01),而mTORC2沉默后,细胞的凋亡率无明显变化(P>0.05);Western印迹检测显示mTORC1沉默后,前列腺癌22RV1细胞中AR和Akt磷酸化表达显著增加(P<0.05),而mTORC2沉默后则显著抑制了前列腺癌22RV1细胞中AR和Akt磷酸化表达(P<0.05)。结论:mTORC2对于前列腺癌22RV1细胞的存活是必需的,mTORC2有可能成为治疗前列腺癌的一个有意义的靶点。
Objective: To explore the role of mammalian target genes of rapamycin mTORC1 and mTORC2 in the proliferation and apoptosis of prostate cancer 22RV1 cells. Methods: MTT assay was used to detect the proliferation of 22RV1 cells after mTORC1 and mTORC2 silencing. Proliferation of 22RV1 cells was detected by flow cytometry (FCM) after silencing mTORC1 and mTORC2. Western blotting was used to detect mTORC1 and mTORC2 silencing Post-prostate cancer 22RV1 cells express androgen receptor (AR) and Akt phosphorylation. Results: After MTT showed mTORC1 silencing, the growth of 22RV1 cells in prostate cancer showed no significant change (P> 0.05). However, mTORC2 silence inhibited the proliferation of cells (P <0.01). After mTORC1 silencing, (P <0.01). However, there was no significant difference in the apoptosis rate of mTORC2 cells after silencing mTORC2 (P> 0.05). Western blotting showed that phosphorylation of AR and Akt in 22RV1 cells was significantly decreased after mTORC1 silencing (P <0.05). However, silence of mTORC2 significantly inhibited phosphorylation of AR and Akt in 22RV1 cells (P <0.05). Conclusion: mTORC2 is essential for the survival of prostate cancer 22RV1 cells, and mTORC2 may be a potential target for the treatment of prostate cancer.